I’ve been (and remain) critical of the use of CVP to determine ‘filling status’ or more accurately volume-responsiveness, even using CVP trends; I’m generally in agreement with Dr Marik’s bold statement that “CVP should not be used to make clinical decisions regarding fluid management”1. However there might now appear to be a way of using CVP for this purpose.

Increasing PEEP in patients undergoing positive pressure ventilation can increase the CVP. It has been demonstrated in a small study of cardiac surgical patients2 that the degree to which a 10cmH2O increase in PEEP changes the CVP correlates with fluid responsiveness. The fluid responsiveness was determined by the change in cardiac output measured by thermodilution after a passive leg raise.

There are a number of limitations to this study that should prevent us from immediately extrapolating this method of determining fluid responsiveness to our ED / critical care patients, but the concept is interesting. This can be added to the growing pile of dynamic measures of circulatory filling.

Background Changes in central venous pressure (CVP) rather than absolute values may be used to guide fluid therapy in critically ill patients undergoing mechanical ventilation. We conducted a study comparing the changes in the CVP produced by an increase in PEEP and stroke volume variation (SVV) as indicators of fluid responsiveness. Fluid responsiveness was assessed by the changes in cardiac output (CO) produced by passive leg raising (PLR).

Methods In 20 fully mechanically ventilated patients after cardiac surgery, PEEP was increased +10 cm H2O for 5 min followed by PLR. CVP, SVV, and thermodilution CO were measured before, during, and directly after the PEEP challenge and 30° PLR. The CO increase >7% upon PLR was used to define responders.

Results Twenty patients were included; of whom, 10 responded to PLR. The increase in CO by PLR directly related (r=0.77, P<0.001) to the increase in CVP by PEEP. PLR responsiveness was predicted by the PEEP-induced increase in CVP [area under receiver-operating characteristic (AUROC) curve 0.99, P<0.001] and by baseline SVV (AUROC 0.90, P=0.003). The AUROC's for dCVP and SVV did not differ significantly (P=0.299).

Conclusions Our data in mechanically ventilated, cardiac surgery patients suggest that the newly defined parameter, PEEP-induced CVP changes, like SVV, appears to be a good parameter to predict fluid responsiveness.

As well as the benefits of cardiovascular stability, maintenance of cerebral perfusion pressure, possibly lowering ICP and providing other neuroprotective benefits, ketamine may have other advantages. These are reviewed in a British Journal of Anaesthesia article from which I’ve selected those benefits of interest to practitioners of emergency medicine and critical care.

Additional Beneficial Effects of Ketamine

the dysphoric, or ’emergence’ reactions associated with ketamine may be reduced by pre-administration or co-administration of sedatives, such as benzodiazepines, propofol, dexmedetomidine, or droperidol.

ketamine potentiates opioid analgesia in multiple settings, reducing opioid total dose and in some groups of patients reducing postoperative desaturation

ketamine has possible anti-inflammatory effects demonstrated in some types of surgical patients

ketamine may prevent awareness, recall, or both during general anaesthesia

The tradition of transporting trauma patients to hospital in a supine position may not be the safest approach in obtunded patients with unprotected airways. The ‘solution’ of having them on an extrication board (backboard / long spine board) to enable rolling them to one side in the event of vomiting may not be practicable for limited crew numbers.

The Norwegians have been including the option of the lateral trauma position in their pre-hospital trauma life support training for some years now.

A questionnaire study demonstrates that this method has successfully been adopted by Norwegian EMS systems.

The method of application is described as:

Check airways (look, listen, feel).

Apply chin lift/jaw thrust, suction if needed.

Apply stiff neck collar.

If the patient is unresponsive, but has spontaneous respiration: Roll patient to lateral/recovery position while maintaining head/neck position.

Roll to side that leaves the patient facing outwards in ambulance coupé.

Different options for supporting the head in the lateral position, according to questionnaire responders, include:

putting padding under the head, such as a pillow or similar item (81%)

a combination of padding and putting the head on the lower arm (7%)

rest the head on the lower arm alone (10%)

rest the head on the ground (<1%)

BACKGROUND: Trauma patients are customarily transported in the supine position to protect the spine. The Airway, Breathing, Circulation, Disability, and Exposure (ABCDE) principles clearly give priority to airways. In Norway, the lateral trauma position (LTP) was introduced in 2005. We investigated the implementation and current use of LTP in Norwegian Emergency Medical Services (EMS).

METHODS: All ground and air EMS bases in Norway were included. Interviews were performed with ground and air EMS supervisors. Questionnaires were distributed to ground EMS personnel.

RESULTS: Of 206 ground EMS supervisors, 201 answered; 75% reported that LTP is used. In services using LTP, written protocols were present in 67% and 73% had provided training in LTP use. Questionnaires were distributed to 3,025 ground EMS personnel. We received 1,395 (46%) valid questionnaires. LTP was known to 89% of respondents, but only 59% stated that they use it. Of the respondents using LTP, 77% reported access to written protocols. Flexing of the top knee was reported by 78%, 20% flexed the bottom knee, 81% used under head padding. Of 24 air EMS supervisors, 23 participated. LTP is used by 52% of the services, one of these has a written protocol and three arrange training.

CONCLUSIONS: LTP is implemented and used in the majority of Norwegian EMS, despite little evidence as to its possible benefits and harms. How the patient is positioned in the LTP differs. More research on LTP is needed to confirm that its use is based on evidence that it is safe and effective.

A review of capillary refill time (CRT) reveals some interesting details about this test:

CRT is affected by age – the upper limit of normal for neonates is 3 seconds.

It increases with age – one study recommended the upper limit of normal for adult women should be increased to 2.9 seconds and for the elderly to 4.5 seconds.

It is affected by multiple external factors (especially ambient temperature).

Although it is claimed to have some predictive value in the assessment of dehydration and serious infection in children, studies vary in where and for how long pressure should be applied, and there is poor interobserver reliability.

The latest (5th Edition) of the Advanced Paediatric Life Support Manual states:
‘Poor capillary refill and differential pulse volumes are neither sensitive nor specific indicators of shock in infants and children, but are useful clinical signs when used in conjunction with the other signs described‘

In my view, it is best used as a monitor of trends (in accordance with skin temperature and other markers of perfusion), rather than by placing emphasis on the exact number of seconds of a single reading. See below for a video of my perfectly happy and healthy son demonstrating a CRT of over six seconds in a cool room during an English Summer’s day.

The authors of the review caution:Operating rooms are cold, patients are often draped, which limits access, and because most anesthetics are potent vasodilators, the use of CRT to guide practice is not justified. The possibility of a false-positive or false-negative assessment is simply too great.

Capillary refill time (CRT) is widely used by health care workers as part of the rapid, structured cardiopulmonary assessment of critically ill patients. Measurement involves the visual inspection of blood returning to distal capillaries after they have been emptied by pressure. It is hypothesized that CRT is a simple measure of alterations in peripheral perfusion. Evidence for the use of CRT in anesthesia is lacking and further research is required, but understanding may be gained from evidence in other fields. In this report, we examine this evidence and factors affecting CRT measurement. Novel approaches to the assessment of CRT are under investigation. In the future, CRT measurement may be achieved using new technologies such as digital videography or modified oxygen saturation probes; these new methods would remove the limitations associated with clinical CRT measurement and may even be able to provide an automated CRT measurement.

It’s become popular to use the term ‘vasopressors’ or just ‘pressors’ when noradrenaline/norepinephrine or even (in some places still) dopamine are given. I have resisted this trend and continue to use the term ‘vasoactive’ drugs, on the basis that the effects they produce (and that we may desire) are not limited to a pure alpha adrenergic effect on vascular tone, but they have effects on heart rate and contractility too (as well as preload through venous effects). If you don’t believe me about noradrenaline/norepinephrine, then check out one of my favourite critical care papers of all time: the CAT study.

There are of course real pressors out there – phenylephrine acts on alpha receptors, as does methoxamine. Metaraminol predominantly acts on alpha receptors but does also cause some release of noradrenaline/norepinephrine.

Why is this important? All these drugs will fix hypotension, right? Yes, they should. However should blood pressure be our main treatment goal? What we’re really interested in is organ perfusion, which depends on regional blood flow to vital organs. It’s possible that a drug could fix the measured blood pressure and give a nice ‘macroscopic’ number, while at the same time reducing cardiac output and adversely affecting regional blood flow to organs through local vasoconstrictive effects. My view is that this is more likely with pure ‘pressors’ (like phenylephrine), which is why I avoid them in septic shock and opt for catecholamine infusions (noradrenaline/norepinephrine).

This is important in my practice setting of retrieval medicine, where, prior to interfacility transport, physicians might sometimes be tempted to ‘push pressors’ peripherally rather than insert a central venous catheter and commence a catecholamine infusion. While the former approach might be more expeditious and make the vital signs chart look pretty, one wonders about what effect this is having on tissue oxygen delivery.

A fascinating review of papers on pressor physiology1 suggests these agents have the following effects:

conflicting data on changes in myocardial perfusion

increase both left and right heart afterload

decrease venous compliance with the potential to increase venous return although the impact of this on cardiac output is controversial

controversial effect on cerebral bloodflow

decrease bloodflow to the kidneys

adverse affects on gastrointestinal tract bloodflow

abstract1
Phenylephrine and methoxamine are direct-acting, predominantly α(1) adrenergic receptor (AR) agonists. To better understand their physiologic effects, we screened 463 articles on the basis of PubMed searches of “methoxamine” and “phenylephrine” (limited to human, randomized studies published in English), as well as citations found therein. Relevant articles, as well as those discovered in the peer-review process, were incorporated into this review. Both methoxamine and phenylephrine increase cardiac afterload via several mechanisms, including increased vascular resistance, decreased vascular compliance, and disadvantageous alterations in the pressure waveforms produced by the pulsatile heart. Although pure α(1) agonists increase arterial blood pressure, neither animal nor human studies have ever shown pure α(1)-agonism to produce a favorable change in myocardial energetics because of the resultant increase in myocardial workload. Furthermore, the cost of increased blood pressure after pure α(1)-agonism is almost invariably decreased cardiac output, likely due to increases in venous resistance. The venous system contains α(1) ARs, and though stimulation of α(1) ARs decreases capacitance and may transiently increase venous return, this gain may be offset by changes in afterload, venous compliance, and venous resistance. Data on the effects of α(1) stimulation in the central nervous system show conflicting changes, while experimental animal data suggest that renal blood flow is reduced by α(1)-agonists, and both animal and human data suggest that gastrointestinal perfusion may be reduced by α(1) tone.

A review of clinical articles2 reveals few evidence-based indications for true pressors. Possible situations where they may be of benefit include intraoperative hypotension, aortic stenosis, during cyanotic episodes in Tetralogy of Fallot, and some obstetric situations. In the setting of sepis, phenylephrine has been compared with noradrenaline in which an initial pilot study found a statistically significant reduction in creatinine clearance and increase in arterial lactate after initiating the phenylephrine infusion. However a subsequent randomised controlled comparison of phenylephrine with noradrenaline/norepinephrine did not show differences in cardiopulmonary performance, global oxygen transport, or regional hemodynamics, although there were only 16 patients in each group3.

abstract2
Phenylephrine is a direct-acting, predominantly α(1) adrenergic receptor agonist used by anesthesiologists and intensivists to treat hypotension. A variety of physiologic studies suggest that α-agonists increase cardiac afterload, reduce venous compliance, and reduce renal bloodflow. The effects on gastrointestinal and cerebral perfusion are controversial. To better understand the effects of phenylephrine in a variety of clinical settings, we screened 463 articles on the basis of PubMed searches of “methoxamine,” a long-acting α agonist, and “phenylephrine” (limited to human, randomized studies published in English), as well as citations found therein. Relevant articles, as well as those discovered in the peer-review process, were incorporated into this review. Phenylephrine has been studied as an antihypotensive drug in patients with severe aortic stenosis, as a treatment for decompensated tetralogy of Fallot and hypoxemia during 1-lung ventilation, as well as for the treatment of septic shock, traumatic brain injury, vasospasm status-postsubarachnoid hemorrhage, and hypotension during cesarean delivery. In specific instances (critical aortic stenosis, tetralogy of Fallot, hypotension during cesarean delivery) in which the regional effects of phenylephrine (e.g., decreased heart rate, favorable alterations in Q(p):Q(s) ratio, improved fetal oxygen supply:demand ratio) outweigh its global effects (e.g., decreased cardiac output), phenylephrine may be a rational pharmacologic choice. In pathophysiologic states in which no regional advantages are gained by using an α(1) agonist, alternative vasopressors should be sought.

These review articles reinforce my own bias against the use of pure pressors in septic shock, although clearly more clinical research is needed. I am inclined to agree with the reviewers’ concluding statement:

…in all clinical settings, phenylephrine reduces cardiac output, and in most clinical settings has been shown to significantly increase LV afterload. Thus, only in instances in which its regional effects are thought to outweigh its global effects should phenylephrine be used for the treatment of hypotension.

STUDY OBJECTIVE: The purpose of this randomized controlled trial was to determine the immediate and delayed effects of noninvasive ventilation for patients in acute cardiogenic pulmonary edema (ACPE) in addition to aggressive usual care in a medical prehospital setting.

METHODS: Out-of-hospital patients in severe ACPE were eligible for the study. Patients were randomized to receive either usual care, including conventional optimal treatment with furosemide, oxygen, and high-dose boluses of isosorbide dinitrate plus oxygen, or conventional medications plus out-of-hospital continuous positive airway pressure (CPAP). The primary outcome was the treatment success defined as all of respiratory rate less than 25 breaths per minute and oxygen saturation of greater than 90% at the end of 1-hour study. Secondary end points included death during 30 days after inclusion. Lengths of intensive care unit and hospital stays were also recorded.

RESULTS: In total, 124 patients were enrolled into the study. The 2 groups had similar baseline characteristics. For the primary outcome analysis, 22 (35.5%) of 62 patients were considered as experiencing a treatment success in the usual care group vs 19 (31.7%) of 60 in the CPAP group (P = .65). Seven patients died within 30 days in the usual care group vs 6 in the CPAP group (P = .52). There were no statistically significant differences between the treatment groups for length of stay either in hospital or in the intensive care unit.

CONCLUSION: In the prehospital setting, in spite of its potential advantages for patients in ACPE, CPAP may not be preferred to a strict optimal intravenous treatment.

The Executive Committee of Prehospital Trauma Life Support, comprised of surgeons, emergency physicians, and paramedics, has reviewed the literature and produced the following recommendations on Prehospital Spine Immobilisation for Penetrating Trauma:

PHTLS Recommendations

There are no data to support routine spine immobilization in patients with penetrating trauma to the neck or torso.

There are no data to support routine spine immobilization in patients with isolated penetrating trauma to the cranium.

Spine immobilization should never be done at the expense of accurate physical examination or identification and correction of life-threatening conditions in patients with penetrating trauma.

Spinal immobilization may be performed after penetrating injury when a focal neurologic deficit is noted on physical examination although there is little evidence of benefit even in these cases.